set point range
a single value that the body works to maintain
ex: calcium level, temperature, water, etc.
weight is regulated tightly within a...
set point range
energy imbalance
when weight consistently increases or decreases
obesity
one of the top 5 health problems - a mass epidemic
many health risks with being over or under weight
body mass index
a measure of body fat
= body weight/ height^2
more than 1 in 3 adults are obese
mortality rates and BMI
thinner people live longer
very thin people do not have the lowest mortality rates,
average BMI has the lowest risk
estimations for BMI
BMI is dependent on weight and height so it makes simplistic
assumptions about distribution of muscle and bone mass
overestimated for more lean body mass - athletes
underestimated for less lean body mass - elderly
central deposition of fat (central obesity)
you have greater health risks if you have excess fat in your waist -
if your waist circumference is more than half your height, you have
dangerous visceral fat
dangers of visceral fat
visceral fat releases toxic substances and causes metabolic diseases
associated with central obesity - hypertension, high cholesterol, type
2 diabetes, coronary heart disease
function of digestive system
to break down food into smaller molecules that the cells can use
how does digestion work
begins in the mouth where saliva enzymes break down carbohydrates
hydrochloric acid and stomach enzymes digest proteins
small intestine enzymes digest proteins, fats and
carbohydrates and absorb the digested food into the bloodstream
large intestine absorbs water and minerals and lubricates
remaining materials to be excreted
homeostasis
controlled stability of the internal environment of cells and tissues
biological processes that keep body variables within a fixed
range or set point
feedback control loops
explained how certain systems work as homeostatic mechanisms
claude bernard
father of modern experimental physiology
-studied digestion and role of pancreas
-understanding of glucose regulation in the liver
discovered neural control of blood vessels
negative feedback processes
processes that reduce discrepancies from the set point
when something becomes off in the body, negative feedback
loops work to bring it back to normal
ex: when you eat, glucose levels rise so insulin is released
to regulate glucose levels
what contributes to hunger and feeding behaviors
a combination of learned and unlearned factors
ex: food selection, hunger, appetite, satiety
hunger
the stimulus that drives our need to eat
when our bodies need fuel, signals are sent from the empty
stomach and intestines that trigger our feelings of hunger
human vs animal strategies of eating
humans tend to eat more than they need
most animals will eat only what they need
alaskan chickadee eats 10% of its body weight per day and
shivers it off at night
bears will eat as much as they can and wont stop so they have
enough storage for hibernation and live off their excess fat
signals of hunger
processed by the brain, but can be overrided
1. delay hunger response actions - people who fast or starve
usually have lower hunger
2. eat more than we need by ignoring satiety receptors that
signal fullness
appetite
a type of signal to eat - can have an appetite for food with or
without hunger
ex: you could have eaten not long ago but sights, smells,
thoughts or discussion of food can stimulate appetite
stress-eating
stressful situations often stimulate appetite (stress-eaters)
food is comforting and those who are experiencing episodic or
chronic stress find comfort in eating
emotionally stressful situations may lead to periods of
binge-like eating in some individuals
satiety
the feeling of fullness that stops appetite and hunger signals
the brain regulates eating through messages from the mouth,
stomach, intestines, fat cells and elsewhere
why is it easy to sometimes overeat
satiety signals that originate in the stomach are delayed from the
start of eating so sometimes you eat more than you need to before
satiety signals are received and acted upon
gastric bypass surgery
the removal or sewing off of part of the stomach
decreased stomach size allows distention of the stomach and
produces satiety sooner
proof that stomach distention is not the only satiety signal
people who have had their stomach removed surgically (ex: cancer)
still report satiety, so signals have to be coming from elsewhere
rather than just the stomach
oral factors of hunger and satiety
the desire to taste and have mouth sensations like chewing cause hunger
people who have a tube in their stomach for feeding report not
feeling satisfied when being fed because they need to chew something
untasted meals are unsatisfying
how are hunger signals affected by the foods you eat
the length of time food stays in the stomach and intestine affects
the duration of satiety and initiation of hunger signals
foods high in protein and fiber vs foods high in fat and processed sugars
foods high in protein and fiber have a high satiety value because
they take longer to digest and stay in the stomach and intestine longer
processed/fatty foods have a low satiety value because they
are easily digested and absorbed readily, they fail to trigger
satiety signals
whole grain products cause people to feel no hunger because
their satiety signals remain on
stomach wall stretching
information conveyed by the vagus nerve to the brain, providing the
major basis for satiety
stomach nutrient content
conveyed by the splanchic nerves
duodenum
the part of the small intestine adjoining the stomach
the first digestive site that absorbs a significant amount of nutrients
releases CCK and GLP-1
CCK and GLP-1
released by the duodenum to restrict flow through the duodenum
causing the stomach to slow gastric emptying and facilitates stomach
distension (the primary signal for ending a meal)
both signal the brain satiety mechanisms
what happens in a healthy person after they eat
glucose levels rise due to the intake in
carbohydrates, if not used, liver cells convert some of the excess
glucose into glycogen for later use and fat cells convert it to fat
insulin levels rise due to the signals of excess
glucose in the body and insulin is released from the pancreas and
enables the glucose to enter the cell - decreases blood glucose and appetite
what happens in between meals
insulin levels are low - hunger is highright before you eat,
insulin is highest and preparing to use the glucose you intake from food
glucose levels are low - glucagon is released and liver cells
convert glycogen back into glucose which returns to the blood and
slows the return of hunger
arcuate nucleus
part of the hypothalamus that has one set of neurons sensitive to
hunger signals, and another set sensitive to satiety signals
damage to the LH results in..
loss of appetite
difference between appetite and hunger
you can have an appetite without being hungry!
appetite is initiated by being hungry, but can also be
stimulated by seeing, hearing, smelling food whether you are hungry
or not
hunger is your body's way of telling you it is actually
hungry, not just an appetite from seeing something delicious
leptin
lowers hunger, highest levels right after you ate a big meal
low leptin levels trigger hunger, high leptin levels trigger satiety
Leptin Lowers hunger
ghrelin
levels increase before a meal to signal hunger and trigger stomach contractions
released by the stomach in a time of food deprivation
the only known hunger hormone
Ghrelin Grows hunger
signals that trigger hunger
taste pathways
decrease in leptin levels
increase in ghrelin
signals that trigger satiety
release of CCK (signal for ending a meal)
increase in leptin levels
rise in blood glucose and insulin
arcuate nucleus pathway for hunger
hunger signals in ARC inhibit the PVH which stimulates the LH to
allow for eating
arcuate nucleus pathway for satiety
satiety signals in ARC stimulate the PVH which inhibits the LH to
stop eating
lateral hypothalamus
facilitates feeding - when stimulated, eating is increased
when inhibited, feeding is stopped
paraventricular hypothalamus
works with (hunger or satiety) signals from the arcuate nucleus to
either stimulate the LH to increase feeding, or inhibit the LH to stop feeding
inhibition of the PVH leads to...
stimulation of the LH and an increase in feeding
stimulation of the PVH leads to...
inhibition of the LH and a stop in feeding
where do all of the signals for feeding occur
in the hypothalamus
inhibitory feeding transmitters
NPY, AgRP and GABA released from hunger signals in the ARC to inhibit
PVH and stimulate LH to stimulate eating
THINK OPPOSITE - inhibitory transmitters stimulate the LH
work on the PVH to excite the LH!!
excitatory feeding transmitters
melanocortin - released from satiety signals in the ARC to stimulate
PVH and inhibit LH to prevent eating
THINK OPPOSITE - excitatory transmitters inhibit the LH
work on the PVH to inhibit the LH!!
leptin hypothesis
high leptin inhibits hunger so some obese persons have a genetic
inability to produce leptin (leptin synthesis deficit) which leads to
more hunger
some obese persons have leptin resistance so they perceive
less leptin than is present and leads to more hunger
melanocortin hypothesis
melanocortin normally excites the PVH to inhibit the LH to stop
eating, some obese persons have a mutated melanocortin receptor gene
so they overeat and become obese because their PVH is not able to
receive the satiety signal
ventromedial hypothalamus (VMH) hypothesis
some persons have damaged VMH leading to excessive eating
increased gastric emptying leads to decreased satiety
increased insulin release and fat storage
both of these effects result in an increase of hunger and eating
emotions can...
enhance communication with other's and with oneself
color experience by focusing one's attention in certain
directions or motivate a person to behave in particular ways
the six basic emotions
anger, sadness, disgust, fear, happy surprise
tripartite mind-body interaction
cognitive awareness of objective events leads to emotional,
physiological and behavioral response
the brain uses ____ to convey the physiological response
autonomic nervous system
4 theories of emotion
common sense theory, james-lange theory, cannon-bard theory,
schacter-singer theory
common sense theory of emotion
emotion comes first, then a specific pattern of autonomic arousal and
skeletal action occurs
frightening situation -> FEAR -> action (running away,
increased heart rate, etc)
"i tremble because i feel afraid
james-lange theory of emotion
autonomic arousal and skeletal actions come first, then we experience
the emotion
frightening situation -> action (running away, increased
heart rate, etc) -> FEAR
main contribution - the experience of emotion may involve
"reading" the state of one's own body
"I feel afraid because i tremble
cannon-bard theory of emotion
emotion is produced in the brain alone, the emotion is mediated via
brain activity following processing of sensory information
emotional cognition, autonomic arousal and skeletal action
occur simultaneously
"the dog makes me tremble and feel afraid
schacter-singer theory of emotion
nonspecific feelings of physiological arousal occur and then
emotional labels are attributed to them
the CNS interprets the current social, physical and cognitive situation
the physiological response is a cue to the brain that something
important may be happening to us
"i label my trembling as fear because i appraise the
situation as dangerous
schacter-singer - the vitamin "suproxin" study
hypothesis: would participants be deceived into experiencing a mood
based on available "cognitive circumstance" in the absence
of an appropriate explanation for arousal?
gave a dose of adrenaline to college students and gave a
placebo to the other and told some of them that the medication was
going to make them aroused. They were placed in a room with a
confederate who was either happy or angry and the ones that were told
they were going to have a physiological response showed anger or
happiness like the confederate in the room with them, placebo showed
no response
what are key components of emotion mechanisms
interpretation of physical states (facial expressions, physiological changes)
what are the critical areas for producing emotion
the limbic system and forebrain
other brain scans have shown areas of the cerebral cortex and
frontal and temporal lobes also activated during an emotional experience
limbic system
the forebrain areas surrounding the thalamus - consists of a number
of interlinked structures that form a border around the brainstem
mediates emotion, motivation, aggression, learning and memory
what did james papez hypothesize
that emotional experience was primarily determined in the cingulate
gyrus and prefrontal cortical regions
but emotional expression is not just the function of one
specific brain center, it is the result of a circuit of limbic system structures
phineas gage
tampering rod went through his brain, took out the connections
between the frontal lobe and the limbic system
used to be a fun, loving guy - then became an aggressive, no
filter, mean guy after the rod took out the connections
showed that higher order structures inhibit lower order
structures - prefrontal cortex could not regulate limbic system so
his emotions were sporadic
how do the limbic system and frontal lobe work together
inhibitory connections from the prefrontal cortex to the limbic
system suppress its emotional suggestions
consequences of damage to the prefrontal cortex
impairs decision making and results in hyper-emotionality (ex:
phineas gage)
loss of prefrontal cortex control leads to impulsive decision
making without considering the consequences
inability to anticipate the unpleasantness of an outcome
ADHD - attention deficit hyperactivity disorder
5% of children or more, 2-3x more in boys
symptoms - distractibility, impulsiveness, hyperactivity
delay in prefrontal cortex cortical development
treated with serotonin reuptake inhibitors to enhance limbic
inhibition and ritalin to block reuptake of dopamine
which hemisphere is more responsive to emotional stimuli
the right hemisphere - listening to laughter or crying activates the
right temporal lobe amygdala more than the left
viewing pictures of emotional facial reactions (anger, fear,
sadness, happiness, disgust) activates the right temporal cortex more
than the left
damage to the right temporal cortex
causes deficits in identifying emotional expressions of others
amygdala
a key structure in the mediation of fear
informs of potential dangers in the environment
many of our body's alarm circuits are grouped together and
linked to the amygdala
function of fear
to alert us of danger
function of anger
directs us to attack an intruder
function of disgust
tells us to avoid something that could cause illness
study with amygdalectomized monkeys
monkeys who had their amygdalas cut out showed higher social
affiliation, lower anxiety, high confidence and lower reluctance to
engage a strange monkey in social behavior
overall, they were less fearful
damage to the amygdala interferes with...
learning of fear responses
retention of previously learned fear responses
interpreting stimuli with emotional responses (ex: a
threatening stimuli)
behavioral medicine
extension of biopsychology toward health, emphasizes the effects of
emotions and other behaviors (diet, exercise, smoking) on health and illness
major focus - relationship between life distress and disease -
potential ways stress may affect disease
stress
non-specific response of the body to any demand made upon it
the process by which we perceive and respond to events that are
perceived as harmful, threatening or challenging
10 leading occupational health problems in the US
each of us experience stress in our daily lives, without it our
lives wouldbe dull but when stress overtaxes our coping resources, it
can damage our health
working hypothesis of the stress-disease relationship
chronic and/or repeated acute stress adversely affects multiple
physiological symptoms and contributes to disease pathophysiology more
readily in susceptible persons
aka - more/repeated stress leads to greater disease
sources of stress
major life events, catastrophes, daily hassles, environmental, job-related
stressor
any event or situation that triggers coping adjustments
allostasis
the adaptive process of achieving stability (homeostasis) through
physiological or behavioral change
can be carried out by alteration internal regulatory systems
is essential for maintaining internal viability and changing conditions
allostatic load
cumulative long-term effects of the body's physiological response to
stress. both repetitive acute and prolonged chronic stressors may contribute
the stress stimulus
common elements to situations that may elevate stress responses in everyone
- novelty- unpredictability- threat to the
ego- loss of control
the stress response - walter cannon
flight or fight response"
showed extensive research on the bodily response to stressors
(ex: temp extremes, oxygen deficit, negative emotions)
the mind and the body are not discrete and unrelated, they
greatly influence each other
stress is a gift to be used wisely, helps people overcome adversity
major emotions involve the excitation of the nervous system
flight or fight response
prepares the body for handling brief emergencies
induced by stress
brought about by the activation of the
hypothalamic-pituitary-adrenal cortex (HPAC) axis and the
sympathetic-adrenal medulla (SAM) axis
hans selye
defined stress as the non-specific response of the body to any demand
made upon it
studied influence of stress on ability to cope with and adapt
to the pressures of injury and disease
discovered that a variety of ailments became apparent with
similar symptoms, attributed to the body's efforts to respond to the
stresses of being ill
general adaptation syndrome
any threat to the body activated a generalized response to stress
eustress" - good stress
when stressors are viewed as challenges, then they can lead to growth
and enhanced functioning
3 stages of general adaptation syndrome
1. alarm stage
2. resistance stage
3. exhaustion stage
alarm stage of general adaptation syndrome
acute increase in sympathetic nervous system activity, readying the
body for brief emergency activity
resistance stage of general adaptation syndrome
sympathetic response declines, adrenal cortex releases cortisol and
other hormones that enable the body to maintain prolonged alertness,
fight infection and heal wounds
highest resistance to stress
exhaustion stage of general adaptation syndrome
occurs after prolonged stress when the nervous and immune systems no
longer have the energy to sustain heightened responses
inactivity, vulnerability and decreased energy to sustain
heightened responses
when is cortisol released
in the resistance stage of the general adaptation syndrome
enables the body to maintain prolonged alertness, fight
infections and heal wounds
activation of general adaptation syndrome
activated by long-term, inescapable factors
in the short term is helpful, in the long term is harmful to health
HPAC axis
hypothalamic-pituitary-adrenal cortex
becomes the dominant response to prolonged stressors
activation of hypothalamus induces the pituitary gland to
secrete adrenocorticotrophic hormone (ACTH)
ACTH stimulates the adrenal cortex to secrete cortisol
ACTH
stimulates the adrenal cortex to secrete cortisol
cortisol
stress hormone"
helps to mobilize energies to combat a difficult situation
levels of cortisol are used as an index of stress - more
cortisol means you're overcoming more stress
the transactional model
richard lazarus - the experience of stress depends as much on how an
event is appraised as it does on the stressor event itself
"our emotions and thoughts are inextricably linked"
when we are presented with a stressor, we appraise the
situation as not harmful, or harmful. if harmful, we cope with it and
deal with the aftereffects and wear and tear
psychoneuroimmunology
study of the relationship of psychological and behavioral factors,
immunity and changes in health status
flight or fight response is driven by...
the central nervous system
ader and cohen study
were studying rats with conditioned taste aversion to a
nausea-inducing drug
gave rats sugar water then injected a nausea inducing drug
later found that the rats were getting very sick and dying
because the taste of the sugar water produced a conditoned response
that produced a weakened immune system
later discovered that the number of virus and infection
fighting immune cells was significantly reduced, this led to proof
that the brain and immune system were connected
2 responses to stress
1. sympathetic (inside autonomic) nervous system is activated - fight
or flight response
2. HPAC axis activated - hypothalamus is activated which
induces the pituitary gland to release ACTH, which then stimulates
the adrenal cortex to release cortisol
exam stress
students had lower antibodies during exam times than during vacations
lonely students
lonely students had poorer immune function than non-lonely students
during exams
perceived stress
exposed subjects to cold virus; those who had 1 month or more of
increased perceived stress were more likely to become infected
nuclear accident
residents within 3 miles of the nuclear accident had lower immune
system function 6 years later relative to those without elevated
perceived stress
effects of long term stress on the immune system
release of substances that injure cells and cause an elevation of
inflammatory cytokines in the body - this produces symptoms of illness
(ex: fever, sleepiness, lack of energy, etc)
sleep and inactivity are the body's way of conserving energy to
fight illness
negative emotions, inflammation and stress
inflammatory substances are linked with depression, fatigue and other
negative emotions
negative emotions contribute greater risk for prolonged
infection and delayed wound healing which further fuels sustained
inflammatory substance release
causes of amnesia
amnesia - the loss of memory
many kinds of brain damage, caused by disease or accident,
impair learning and memory and cause amnesia
anterograde amnesia
the inability to form new memories after the event that caused the amnesia
retrograde amnesia
loss of memory for information occurring prior to the event that
caused the amnesia
HM study
underwent an experimental brain surgery for seizures and after the
surgery he could not make any new memories (suffered from anterograde amnesia)
surgery was a bilateral temporal lobe resection, which included
amygdala and some surrounding cortex
could not make new memories or every day events and could not
learn new information, but had good short term memory
did not suffer from any intellectual or personality disorders,
despite his amnesia
outcome of HM study
because HM only suffered from anterograde amnesia and did not lose
any of his short term memory, past memory, personality or intellectual
ability, researchers hypothesized that the hippocampus was necessary
for forming new memories, but may not be where new memories are stored
job of the hippocampus
to serve memory consolidation for declarative memory, not LTM storage
memory consolidation is transferring short term memory into long
term memory
hippocampus damage
in the case of HM or a lesion - it impairs recent learning more than
older learning
people with hippocampus damage can learn new skills but have a
hard time learning new facts
delayed non-matching-to-sample task
a declarative memory task - an animal must learn that of the two
objects, the food is under the one it had not seen 10 minutes before
when the animal has hippocampus damage, they are still able to
learn the correct response when there is no delay, but damage impairs
their memory consolidation, causing forgetting after 10 minutes
declarative (explicit) memory
facts and info acquired through learning that can be consciously recalled
we are aware of this info and we can declare or verbalize it to
others - deals with "what
nondeclarative (implicit or procedural) memory
previous experiences aid the performance of a task without conscious
awareness of these previous experiences.
memory about perceptual or motor procedure, demonstrated by
performance rather than by conscious recollection - deals with the "how
2 types of declarative memory
episodic - recalling a specific episode in your life
semantic - basic facts acquired over a lifetime
3 forms of nondeclarative memory
skill learning
priming
conditioning
skill learning
type of nondeclaritive memory
learning to perform a series of procedures that requires motor coordination
ex: people were told to trace an image but can only see the
mirror reflection. normal people improved with practice, people
with deficits in nondeclarative memory could not show improvement
with practice
priming (repetition priming)
type of nondeclaritive memory
improvements in a behavioral response when stimuli are
repeatedly presented
or: exposure to a stimulus facilitates or speeds subsequent
responses to the same/similar stimulus
conditioning
type of nondeclaritive memory
learning simple associations between two stimuli, or a stimulus
with a response
pavlovian or operant
classical (pavlovian) conditioning
the pairing of two stimuli changes the response to one of them
UCS automatically leads to UCR, but with repeated pairing of the
CS with the UCS, soon the CS will produce the CR
think pavlov's study with dogs and salivation
operant conditioning
responses are followed by reinforcement or punishment that either
strengthen or weaken the probability of the behavior occurring in the future
positive and negative reinforcers are events that increase the
probability of the response occurring again
punishments are events that decrease the probability that the
response will occur again
think watson and skinner
short term memory
memory of events that have just occurred
STM retains info for less than a minute if attention is paid to
the elements in sensory register
repetition keeps the info available longer
long term memory
memory of events from times further back
memory trace - a persistent change in the brain that reflects
the storage of info
neuronal activities continue even after the termination of the
stimulus - inducing structural changes
different neurons are linked via this activity and form neural
circuits that can fire in specific patterns with minimal stimulation
sensory memory
briefest memories are called iconic (visual) and echoic (auditory) memories
they are fleeting impressions that vanish within a second,
thought to be residual sensory perceptions
3 aspects of info processing for a functional memory system
encoding of raw info from sensory channels into STM
consolidation of volatile STM traces into more
durable LTM
retrieval of stored info for use in future behavior
problem with any of these leads to forgetting
working memory (central executive)
responsible for the transient holding and processing of new and
already stored information; integral for reasoning, comprehension and
learning and memory
lashley's search for the engram
engram - the physical representation of what has been learned
lashley trained rats on different mazes and then cut or removed
various parts of their brains to see if any cuts or lost parts would
cause them to forget how to do the maze. his research led him to
believe that
1. all parts of the cortex contribute equally to learning and
complex behaviors and
2. the cortex works as a whole, and more cortex is better
researchers later discarded these assumptions with more research
studies of memory retrieval
show that memory retrieval from LTM causes memories to become
temporarily unstable and susceptible to disruption or alteration
before reconsolidation
ex: people recalling facts for a jury
but using memories again makes them plastic again and
suscepitble to updating
hippocampus and context
hippocampus is involved in cognitive processing of space, time and
the relationships of external cues occurring at the time of an
event...contextual learning
ex: remembering the detail and context of an event
cognitive map
term is coined by tolman
studied learning using mazes and rats
concluded that learning did not result strictly from a stimulus
and a response - but rather through more subtle differences of
processing of info where prior experiences and connections could be
applied to new situations
hippocampus damage impairs spatial learning
test used to asses spatial ability in rodents
radial maze - navigate a maze with 8 or more arms, with a reinforcer
at the end of selected arms
studies showed that animals do not just learn a series of turns,
but instead develop a cognitive map to do the maze
radial arm maze
8 arms with food at a selected few - tested rodents with and without
hippocampus damage to see if they could remember which arms they
already went to to get food
must use extra-maze cues to determine which arms have been
entered during a particular trial (STM) and enter each baited arm
only once following training (tests working/LTM)
results of radial arm maze with rats
separate trained rats underwent lesioning in several different parts
of the brain including the hippocampus, but only rats with damage to
the hippocampus were impaired
place cells fire in radial maze study to show rats where they
are relative to the environment - this lets them see where they've
been and where they haven't
cognitive map
a mental representation of the spatial layout of an environment made
up of boundary, place and grid fields
boundary cells-fire when a person is located near the geographic
limit of the space they are in
place cells-fire when persons occupy a particular location
relative to the arrangement of objects within an environment
grid cells-fire when the person is in, or moving toward, a
particular location
prefrontal cortex and anterior cingulate cortex involvement in
learning and memory
liked to learning about rewards and punishments
parietal lobe secondary cortex involvement in learning and memory
associated with piecing sensory and motor information together
anterior and inferior region of the temporal cortex involvement in
learning and memory
associated with semantic memory (meaning of words) and object recognition
erik kandel
studied the gill and siphon withdrawal reflexes in aplysia, chose
aplysia because of the simplicity and relatively large size of the
neural circuitry
studied habituation, dishabituation and sensitization
results of kandel's study with aplysia
provided solid evidence for the mechanistic basis of learning as
"a change in the functional effectiveness of previously existing
excitatory connections
hebbian synapse
when two neurons fire at the same time, they become strengthened and
more likely to fire again in the future
cells that fire together, wire togethercells that fire
apart, wire apart
occurs when the successful stimulation of a cell by an axon leads
to the enhanced ability to stimulate that cell in the future
increased effectiveness of synaptic function occurs because:
a. increase in presynaptic transmitter release improves
nondeclarative STM b. increase in number of
post-synaptic receptors improves declarative STM
c. increased number of synapses improves LTM
long-term potentiation (LTP)
the enlargement of the graded potential; a mechanism of declarative LTM
when a number of axons are all firing on a dendrite for a period
of time, the neuron becomes more responsive to input of the same type
for a certain period of time
habituation
a decrease in response to a stimulus that is presented repeatedly
kandel ex: if you repeatedly stimulate an aplysia's gills with a
jet of seawater, at first it will withdraw, but eventually it will
stop responding
sensitization
an increase in response to mild stimuli as a result of exposure to
more intense stimuli
kandel ex: a strong stimulus almost anywhere on aplysia's skin
intensifies a later withdrawal response to a touch
specificity
if some of the synapses of a cell have been highly active and others
have not, only the active ones become strengthened
cooperativity
simultaneous stimulation by 2 or more axons produces LTP much more
strongly than repeated stimulation by a single axon
associativity
pairing a weak input with a strong input enhances later responses to
a weak input
biochemical mechanisms of LTP
the pre-synaptic neuron releases lots of glutamate which binds to the
AMPA receptors on the post-synaptic neuron.
this extreme depolarization allows the magnesium blocking the
nearby NMDA receptor to displace, and glutamate to binds to the NMDA
receptors which allow sodium to flow through both AMPA and NMDA
receptors, and calcium to flow through NMDA receptors
this causes more post-synaptic receptors and more axons are made,
which allows for greater stimulaiton later on
this established LTP
short-term synaptic changes of LTP
repeated glutamate excitation causes more AMPA and NMDA receptors to
be made and put onto the surface of the post-synaptic neuron
this increases the responsiveness of the receptors on the
post-synaptic dendrite to incoming glutamate which leads to increased
synaptic strength
long-term synaptic changes of LTP
in response to the increased stimulation of a postsynaptic cell
learning and memory involves:
pre-synaptic cell changes - more neurotransmitters are released,
decrease in action potential threshold
post-synaptic cell changes - expansion of membrane - more
receptors and axons
more neurotransmitters can be released from more sites and
received at more sites
korsakoff's syndrome
more common in alcoholics - causes them to lose vitamins they need to
metabolize glucose, so neurons in the brain shrink
this causes damage to the prefrontal cortex leading to memory
loss and confusion, similar to those with hippocampal damage,
impairment of episodic and sparing of implicit memory
major symptom is confabulation - where they fill in missing
memories with wrong ones
alzheimer's disease
have better procedural than declarative memory, they learn new skills
but then surprise themselves at their skills because they don't
remember learning those skills
neurons weaken and die with causes memory loss
what stimulates an LTP
repeated huge release of neurotransmitters from a strong action potential
benefits of greater surface area following LTP
greater opportunity for receptors, collateral sprouting, axonal
endings � all part of synaptogenesis, when we are learning and storing
information, all of that is accompanied by structural changes in the brain
consciousness
the private awareness we have of our emotions, intentions, thoughts,
sensations and movements
right now we cant stimulate parts of the brain to induce consciousness
machines cant be brought to experience awareness
consciousness exists in certain parts of certain kinds of nervous systems
we can only be aware of 1-2 thoughts at a time, so most of our
processing is non-conscious
neural correlates of consciousness
the relationship between the experiences reported by subjects and the
activity that simultaneously takes place in their brains
why do researchers study apes so much
they resemble many human characteristics
form social hierarchy relationships and exhibit competition for resources
this shows the evolution of intelligence
self-awareness
we are aware of ourselves and others and can learn about ourselves
from others' behavior
the product of a diffuse patchwork of key cortical regions
mirror and rouge task - put a mark on animals and humans to see
if they are able to recognize that the mark is actually yon
themselves and they can notice it
cerebral asymmetry
the idea that each brain hemisphere is specialized for different functions
right vs left hemisphere - perform different but complementary functions
left side is specialized for
logical/linear thinking, language, writing, science and math, speech
became specialized for handedness and then developed speech
right side is specialized for
musical and artistic ability, perception of space, imagination and
fantasizing, body control and awareness
3D space and more creative/abstract
thought to have specialized for the purpose of detecting and
responding to unexpected stimuli
essential for recognizing predators quickly, face recognition,
analyzing spatial relationships
washoe
the chimp that learned to sign and even went on to teach other chimps
to sign
used mainly his right hand, this shows that they have selective
reliance on the left side just like humans do
ability of bonobos
resemble humans more than any other primates
show better comprehension of human language
understand more than they can produce, use symbols/names to
describe objects, request items not seen, use symbols to describe
past events, make original creative requests
aphasia
a condition in which there is severe language impairment
broca's aphasia (nonfluent aphasia)
a speech production deficit unrelated to auditory
dysfunction, people with brain damage suffer impaired language production
people who are deaf cannot make meaningful speech, but that is
related to an auditory dysfunction, not to a problem in Broca�s area (aphasia)
main problem in broca's aphasia
they have a problem with understanding when sentence structure is complicated
they have a problem in moving the muscles to
produce speech, not a comprehension problem
wernicke's aphasia (fluent aphasia)
speech comprehension deficit unrelated to auditory dysfunction
poor language comprehension and impaired ability to remember
names of objects
can still speak smoothly, damage to secondary auditory cortex
characteristics of wernicke's aphasia
articulate speech - speak smoothly except when they have to remember
the name of something
difficulty finding the right word (anomia) - ex:
they use thingamajig or "the thing we use to sweep"
poor language comprehension - trouble understanding spoken and
written speech
agrammatism
a lack of use of syntax in speech production and comprehension
speech requires great effort
anomia
difficulty recalling the names of objects, especially nouns
paraphasia
words may be meaningless combinations of syllables
pronunciation in broca's vs wernickes aphasia
brocas - poor
wenickes - unimpaired
content of speech in broca's vs wernickes aphasia
brocas - mostly nouns and verbs, omits prepositions and other
grammatical connectives
wernickes - grammatical but nonsensical, has trouble finding the
right word, especially nouns
comprehension in broca's vs wernickes aphasia
brocas - impaired if the meaning depends on complex grammar
wernickes - seriously impaired
conduction aphasia
a patient can both comprehend and articulate language, but cannot
verbalize what is a clear idea in their mind
geschwind disconnection theory
deficits can be understood as breaks in an interconnected network of
components, each is involved with a particular feature of language
analysis or production
corpus callosum
a set of axons that allow exchange of information between the left
and right hemispheres
right knows what the left is doing, and vice versa
split-brain operation
cut the corpus callosum to prevent epileptic seizures from spreading
to the opposite side of the brain
optic chiasm
part of the brain where half of the axons from each eye cross to the
opposite side of the brain
this allows info received from the left visual field to be
processed in the right, and info from the right visual field to be
processed on the left
lateralization
division of labor between the two hemispheres of the brain
split brain patients
had their corpus callosum cut, but have two independent streams of consciousness
when a stimulus is presented in the right visual field, the
stimulus is transmitted to the visual area in the left hemisphere and
the person can recognize the stimulus
when a stimulus is presented in the left visual field, the
stimulus is transmitted to the visual area in the right hemisphere,
and the person cannot say what they see
however, motor and somatosensory areas of the right hemisphere
aloow the person to pick up or point to the object represented in the
stimulus with their left hand
inter-manual conflit
occurs in split brain patients when the hands act at cross-purposes -
left hand behaves in a "foreign or alien" manner
ex: woman trying to pick out dress, right and left hand pick 2
different dresses and she is unable to decide which to choose
confabulation
filling in memory gaps with guesses
ex: video we watched of split brain patient guessing what the
woman was doing in the picture she saw that was presented on the left
side. she guessed jumprope when the woman was actually on the phone
we fill in the gaps with the best guess in the absence of information
cross-cueing
when the right hemisphere communicates using non-verbal behavior with
the left hemisphere
ex: when "clap : laugh" was presented, the lady did both,
but did not realize she was clapping
why should the right side not be regarded as the minor hemisphere
it has different abilities, not less important ones
sequential similar
cognitive processes in time are blended and then perceived as one -
putting together static images into a sequence, our brain pieces it together
ex: pictures of little girl laughing and not laughing
sequential dissimilar
processes in time are assessed independently
ex: pictures of little girl laughing and then a picture of an old lady
we are able to recognize that the picture of the old lady does
not fit with the sequence of the rest of the pictures
Agenesis of corpus callosum
people born without a corpus callosum, but still function normally
where do awareness and comprehension occur
Awareness occurs in primary associative cortex
Comprehension in secondary associative cortex
the illusion of knowledge
Your brain creates the illusion that you know more that you actually
do so you can handle the things that come at you
this is a survival mechanism to make us feel more in control
attention
the ability to increase or decrease activity of the engaged neurons
functioning to process the stimulus scene
selective attention
only reacting to certain stimuli and ignoring others when several are
presented simultaneously in order to accomplish tasks
rapid attentive systems
noticeable, readily perceived stimuli
transmitted from lower to high order (bottom-up)
ex: you see a bear, and the information that you just saw a bear is
sent up to your brain (amygdala, motor cortex), where you realize that
you are scared and need to run
slow attentive system
our brain making use of information that has already been brought
into the brain by other sensory systems
controlled from higher to lower order (top-down)
attentive biasing
involves increasing activity in some neural networks and decreasing
it in others - a top-down process
what parts of the brain control attention
the prefrontal cortex and secondary sensory associative cortex
fate of an unattended stimulus
some things capture your attention faster than other things (ex:
name, special word)
if a meaningful stimulus captures your attention faster than a
meaningless stimulus, somehow your brain had to know that it was
meaningful before it became conscious - shows that most brain activity
is unconscious, and even unconscious activity can influence behavior
spatial neglect
after brain damage to the right side - people are unable to notice or
be aware that there is something on their left
pathway of speech production
1. Sound comes in through the ear and sent to wernicke�s area
2. Sent to Broca�s area where sounds are broken apart
3. Sent to primary motor cortex, where the speech is then produced
major depressive disorder
feel sad and helpless every day for weeks at a time, little energy,
feel worthless, contemplate suicide, find little pleasure, cant
imagine being happy
schizophrenia
a deteriorating ability to function in everyday life, and have
experienced delusions, hallucinations, disorganized speech and
behavior, absent emotion and socialization for more than 6 months
literally means "split-mind" but it is
not multiple personalities!
prevalence of schizophrenia
less than 1% of the population
cost in US exceeds cost of all cancers
more common in US and Europe than in 3rd world countries
severity is highly variable
2 types of schizophrenia
acute - condition has a sudden onset and good prospect for recovery
chronic - condition has a gradual onset, a long-term course and
poor prognosis
3 types of schizophrenic symptoms
positive, negative and cognitive
positive symptoms of schizophrenia
behaviors that are present that should be absent
ex: delusions, hallucinations, irrational thoughts
negative symptoms of schizophrenia
behaviors that are absent or diminished but should be present
ex: socialization, infrequent speech, absent emotion
these symptoms are usually stable over time and difficult to treat
cognitive symptoms
deficits in higher cerebral functioning; closely related to negative
symptoms and are characterized by higher cognitive difficulties
ex: poor problem solving, learning and memory, and abstract
thinking; difficulty sustaining attention; low psychomotor speed on
tasks where fingers/hands must move rapidly
types of positive symptoms in schizophrenia
psychotic - delusions and hallucinations
delusions - unfounded beliefs (god-like power) and persecution or
control (belief that someone is after them or trying to control them)
disorganized - inappropriate emotional displays, bizarre
behaviors, thought disorders (disorganized, irrational thinking;
difficulty in logic and sorting out plausible conclusions from absurd
choices; jump from one topic to the next in conversation)
symptom order of schizophrenia
negative symptoms -> cognitive symptoms -> positive symptoms
time course of schizophrenia
symptoms usually appear gradually over 3-5 years
hypothesis for abnormal brain development in schizophrenics
abnormalities in prenatal or neonatal development of the CNS leads to
subtle abnormalities of brain anatomy and major abnormalities in behavior
abnormalities could result from 1. genetics2. trouble
during prenatal/postnatal development or birth3. environmental
influences later in life
genetics/heritability of schizophrenia
appears to be heritable
monozygotic twins have a higher concordance rate than dizygotic
twins (48/17) but because it's only 48%, either there is one gene that
is influenced by other factors that increase susceptibility of it
being triggered, or multiple genes
the dopamine (DA) hypothesis of schizophrenia
positive symptoms are caused by an over-activity of dopamine neurons
in neural pathways connecting the ventral tegmentum to the nucleus
accumbens in the basal forebrain and then to the prefrontal cortex
when anti-DA medication (which has anti-anxiety side effects) were
used on schizophrenic patients, these medications relieved the symptoms
drug treatment: dopamine antagonists/agonists
thorazine is a dopamine antagonist (blocker) used to treat
schizophrenia, blocks dopamine receptors so positive symptoms can be lessened
L-DOPA, cocaine and amphetamines are dopamine agonists that have
an opposite effect and worsen positive symptoms
increased activity at the dopamine receptor in nucleus accumbens
drives positive symptoms
glutamate hypothesis
deficient NMDA receptor stimulation (by glutamate/glutamine) in the
glutaminergic neurons of the prefontal cortex may result in
over-activity (of neuronal response) of the tegmental-forebrain DA pathway
hence, low NMDA receptor stimulation results in increased symptoms
in schizophrenics
proof of glutamate hypothesis
PCP is an antagonist of NMDA receptors in the prefrontal cortex,
large PCP doses produce positive, negative and cognitive schizophrenic symptoms
neural connection for schizophrenic symptoms
lower activation (hypoactivity) of NMDA pathways in prefrontal cortex
(causes negative and cognitive symptoms) leads to greater activation
(hyperactivity) of forebrain dopamine pathways (causes positive symptoms)
non-genetic influences for depression
infections, hormones and stress
what helps depression
anti-depressant drugs (SSRI's and trycyclics) that block reuptake of
dopamine, norepinephrine and serotonin - effectiveness could be due to
placebo effect, or normal recovery over time
electroconvulsive therapy - an electrically induced seizure. lasts
for a few months but could lead to brain damage if done wrong
bipolar disorder
alternating between two poles - depression and mania
depression - sadness, helplessness, litte worthmania -
excitement, laughter, self-confidence, loss of inhibitions
seasonal affective disorder
depression the recurs during a particular season
most prevalent in the poles where there are long nights, most often
caused by a mutation in genes that regulate circadian rhythms